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BCL-2 family in retinal degeneration in ischemia/reperfusion injury and in the RCS rats.

Chiu Kin. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 100-116). / Abstract also in Chinese. / TABLE OF CONTENTS --- p.I / ACKNOWLEDGEMENTS --- p.V / LIST OF FIGURES --- p.VI / LIST OF ABBREVIATIONS --- p.VIII / ABSTRACT --- p.1 / Chapter 1. --- INTRODUCTION --- p.5 / Chapter 2. --- LITERATURE REVIEW --- p.7 / Chapter 2.1 --- RETINAL ISCHEMIA --- p.7 / Chapter 2.1.1 --- INDUCTION OF RETINAL ISCHEMIA --- p.7 / Chapter 2.1.2 --- MECHANISMS OF RETINAL ISCHEMIA/REPERFUSION DAMAGE --- p.8 / Chapter 2.1.2.1. --- Free radical --- p.8 / Chapter 2.1.2.2 --- Excitotoxicity --- p.9 / Chapter 2.1.3 --- APOPTOSIS IN RETINAL ISCHEMIA/REPERFUSION INJURY --- p.10 / Chapter 2.2 --- RETINAL DYSTROPHIC ROYAL COLLEGE OF SURGEONS (RCS) RAT --- p.15 / Chapter 2.3 --- BCL-2 FAMILY MEMBERS --- p.16 / Chapter 2.3.1 --- FAMILY MEMBERS AND THEIR INTERACTIONS --- p.16 / Chapter 2.3.2 --- SUBCELLULAR LOCALIZATION --- p.18 / Chapter 2.3.3 --- PHYSICAL STRUCTURE AND PORE FORMATION --- p.19 / Chapter 2.3.4 --- BIOLOGICAL EFFECTS OF BCL-2 --- p.20 / Chapter 3. --- OBJECTIVES --- p.24 / Chapter 4. --- MATERIALS AND METHODS --- p.27 / Chapter 4.1. --- RETINAL ISCHEMIA AND REPERFUSION INDUCED LOSS OF INNER RETINAL ELEMENTS --- p.27 / Chapter 4.1.1. --- TISSUE RESPONSES IN THE RAT RETINAS AFTER TRANSIENT ELEVATED INTRAOCULAR PRESSURE INDUCED RETINAL ISCHEMIA/REPERFUSION INSULT --- p.27 / Chapter 4.1.1.1. --- Induction of retinal ischemia/reperfusion insult with transient elevated intraocular pressure (IOP) --- p.27 / Chapter 4.1.1.2. --- Animal experiments --- p.28 / Chapter 4.1.1.3. --- Histopathology and measurement of inner retinal thickness (IRT) --- p.28 / Chapter 4.1.1.4. --- Flat preparation of the retinas and retinal ganglion cell counts (RGCCs) --- p.29 / Chapter 4.1.2. --- INTERNUCLEOSOMAL DNA FRAGMENTATION AND IN SITU NICKED DNA DETECTIONS AT DIFFERENT TIME AFTER REPERFUSION IN THE RAT RETINAS --- p.30 / Chapter 4.1.2.1. --- Enzyme-linked immunosorbent assay (ELISA) of mono- and oligonucleosomes --- p.30 / Chapter 4.1.2.2. --- In-situ terminal deoxynucleotidyl transferase (TdT)-mediated biotin- dUTP nicked end labelling (TUNEL) --- p.31 / Chapter 4.1.3. --- "IMMUNOHISTOCHEMISTRY OF BCL-2, BAX AND P53" --- p.32 / Chapter 4.1.4. --- "DOUBLE LABELLING OF BCL-2, BAX AND TUNEL" --- p.33 / Chapter 4.1.5. --- IN-SITU REVERSE TRANSCRIPTASE - POLYMERASE CHAIN REACTION OF BCL-2 AND BAX --- p.34 / Chapter 4.1.5.1. --- Primers design and specificity test --- p.34 / Chapter 4.1.5.2. --- In-situ RT-PCR --- p.36 / Chapter 4.2. --- LOSS OF INNER RETINAL ELEMENTS IN THE RETINAL DYSTROPHIC ROYAL COLLEGE OF SURGEONS (RCS) RATS --- p.38 / Chapter 4.2.1. --- HISTOPATHOLOGY --- p.38 / Chapter 4.2.2 --- MORPHOMETRY OF CELLS IN THE RETINAL GANGLION CELL LAYER (RGCL) AND THE INNER NUCLEAR LAYER (INL) --- p.39 / Chapter 4.2.3. --- IMMUNOHISTOCHEMISTRY OF BCL-2 AND BAX --- p.39 / Chapter 5. --- RESULTS --- p.40 / Chapter 5.1. --- RETINAL ISCHEMIA AND REPERFUSION INDUCED LOSS OF INNER RETINAL ELEMENTS --- p.40 / Chapter 5.1.1. --- TISSUE RESPONSES IN THE RAT RETINAS AFTER TRANSIENT ELEVATED INTRAOCULAR PRESSURE INDUCED ISCHEMIA/ REPERFUSION INSULT --- p.40 / Chapter 5.1.1.1. --- Histopathology --- p.40 / Chapter 5.1.1.2. --- Morphometry of inner retinal thickness --- p.40 / Chapter 5.1.1.3. --- Retinal ganglion cell counts (RGCCs) --- p.41 / Chapter 5.1.2. --- INTERNUCLEOSOMAL DNA FRAGMENTATION AND IN SITU NICKED DNA DETECTION AT DIFFERENT TIME AFTER REPERFUSION IN THE RAT RETINAS --- p.41 / Chapter 5.1.2.1. --- Enzyme-linked immunosorbent assay (ELISA) of mono- and oligonucleosomes --- p.42 / Chapter 5.1.2.2. --- In situ TUNEL --- p.42 / Chapter 5.1.3. --- BCL-2 AND RETINAL ISCHEMIA/REPERFUSION INJURY --- p.42 / Chapter 5.1.3.1. --- Immunohistochemistry of Bcl-2 --- p.42 / Chapter 5.1.3.2. --- Double labelling of Bcl-2 and TUNEL --- p.43 / Chapter 5.1.3.3. --- In situ RT-PCR for bcl-2 mRNA --- p.43 / Chapter 5.1.4. --- BAX AND RETINAL ISCHEMIA/REPERFUSION INJURY --- p.44 / Chapter 5.1.4.1. --- Immunohistochemistry of Bax --- p.44 / Chapter 5.1.4.2. --- Double labelling of Bax and TUNEL --- p.45 / Chapter 5.1.4.3. --- In situ RT-PCR for bax mRNA --- p.45 / Chapter 5.1.5. --- P53 IMMUNOREACTIVITY AT VARIOUS TIME AFTER REPERFUSION --- p.46 / Chapter 5.2. --- LOSS OF INNER RETINAL ELEMENTS IN THE RETINAL DYSTROPHIC ROYAL COLLEGE OF SURGEON (RCS) RATS --- p.47 / Chapter 5.2.1. --- HISTOPATHOLOGY --- p.47 / Chapter 5.2.2. --- MORPHOMETRY OF CELLS IN THE RGCL AND INL --- p.47 / Chapter 5.2.3. --- IMMUNOHISTOCHEMISTRY OF BCL-2 AND BAX --- p.47 / Chapter 5.2.3.1. --- Bcl-2 --- p.47 / Chapter 5.2.3.2. --- Bax --- p.48 / Chapter 6. --- DISCUSSION --- p.49 / Chapter 6.1. --- RETINA ISCHEMIA AND REPERFUSION INDUCED LOSS OF RETINAL ELEMENTS --- p.51 / Chapter 6.1.1 --- REPERFUSION TIME DEPENDENT TISSUE RESPONSES IN RAT RETINAS --- p.51 / Chapter 6.1.2 --- ISCHEMIA/REPERFUSION INDUCED APOPTOSIS IN RAT RETINAS --- p.52 / Chapter 6.1.3 --- BCL-2 AND RETINAL ISCHEMIA/REPERFUSION INSULT --- p.53 / Chapter 6.1.4 --- BAX AND RETINAL ISCHEMIA/REPERFUSION INSULT --- p.58 / Chapter 6.1.5 --- P53 AND RETINAL ISCHEMIA/REPERFUSION INJURY --- p.60 / Chapter 6.2. --- LOSS OF INNER RETINAL ELEMENTS IN THE RETINAL DYSTROPHIC ROYAL COLLEGE OF SURGEON (RCS) RAT --- p.61 / Chapter 6.2.1. --- HISTOPATHOLOGY AND MORPHOMETRY --- p.62 / Chapter 6.2.2. --- BCL-2 --- p.63 / Chapter 6.2.3. --- BAX --- p.64 / Chapter 7. --- CONCLUSION --- p.65 / APPENDIX A FIGURES --- p.66 / APPENDIX B REFERENCES --- p.100

Identiferoai:union.ndltd.org:cuhk.edu.hk/oai:cuhk-dr:cuhk_322517
Date January 1998
ContributorsChiu, Kin., Chinese University of Hong Kong Graduate School. Division of Surgical Sciences.
Source SetsThe Chinese University of Hong Kong
LanguageEnglish, Chinese
Detected LanguageEnglish
TypeText, bibliography
Formatprint, x, 116 leaves, [20] leaves of plates : ill. (some col.) ; 30 cm.
RightsUse of this resource is governed by the terms and conditions of the Creative Commons “Attribution-NonCommercial-NoDerivatives 4.0 International” License (http://creativecommons.org/licenses/by-nc-nd/4.0/)

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